ICAM-1 and β2 integrin deficiency impairs fat oxidation and insulin metabolism during fasting

Aleksandar M. Babic, Hong Wei Wang, Margaret J. Lai, Thomas G. Daniels, Thomas W. Felbinger, Peter C. Burger, Alain Stricker-Krongrad, Denisa D. Wagner

Research output: Contribution to journalArticlepeer-review


Intercellular adhesion molecule 1 (ICAM-1) and β2 integrins play critical roles in immune responses. ICAM-1 may also participate in regulation of energy balance because ICAM-1-deficient mice become obese on a high-fat diet. We show that mice deficient in these adhesion receptors are unable to respond to fasting by up-regulation of fatty acid oxidation. Normal mice, when fasted, exhibit reduced circulating neutrophil counts and increased ICAM-1 expression and neutrophil recruitment in liver. Mice lacking ICAM-1 or β2 integrins fail to show these responses-instead they become hypoglycemic with steatotic livers. Fasting ICAM-1-deficient mice reduce insulin more slowly than wild-type mice. This produces fasting hyperinsulinemia that prevents activation of adenosine mono-phosphate (AMP)-activated protein kinase in muscles and liver, which results in decreased import of long chain fatty acids into mitochondria. Thus, we show a new role for immune cells and their adhesion receptors in regulating metabolic response to fasting.

Original languageEnglish (US)
Pages (from-to)72-79
Number of pages8
JournalMolecular Medicine
Issue number7-12
StatePublished - Jul 2004
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Genetics(clinical)


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